SBA Answers and Explanations
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury in SBAs for the MRCS Part A, 2018
Respiratory acidosis occurs when there is a decreased ventilation (hypoventilation) which results in an increase concentration of carbon dioxide in the blood and a decrease in the blood pH. Alveolar hypoventilation results in an increased PaCO2, which in turn decreases the HCO3−/PaCO2 ratio and decreases the pH. Acute respiratory acidosis occurs when there is an abrupt failure of ventilation. This failure can be caused by depression of the central respiratory centre by central nervous/cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction (e.g., asthma). Moreover, chronic respiratory acidosis can occur with the following condition: (e.g., chronic obstructive pulmonary disorder), obesity hypoventilation syndrome (i.e., Pickwickian syndrome), neuromuscular disorders (e.g., amyotrophic lateral sclerosis) or related to severe restrictive ventilatory defects (e.g., interstitial lung disease and thoracic deformities).
Control of Respiration
Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod in The Primary FRCA Structured Oral Examination Study Guide 1, 2017
Describe the effects of raised CO2 on the body. Hypercarbia stimulates respiration via activation of peripheral and central chemoreceptors.CVS – systemic vasodilatation, myocardial depression and arrhythmias.Pulmonary circulation – increased pulmonary vascular resistance. Respiratory acidosis.CNS – stimulates respiration but at high levels causes narcosis. Increases cerebral blood flow and intracranial pressure.Renal – slower compensation via bicarbonate retention and urinary hydrogen ion excretion.
Fluid and electrolyte balance in the newborn
Prem Puri in Newborn Surgery, 2017
Patients who have been adequately managed pre- and intraoperatively may be well hydrated, immediately, postoperatively. If the infant had hypotension, transient renal failure with oliguria may occur and may be managed with fluid restriction and correction of electrolyte abnormalities. Inappropriate secretion of antidiuretic hormone is common and results from pain and/or ventilation, resulting in fluid retention and hyponatremia; thus, care must be taken to avoid overhydration, which will encourage both of these. Respiratory acidosis should be corrected by appropriate ventilation. Metabolic acidosis may occur postoperatively in the infant who is persistently hypotensive or hypoxic or who has ongoing tissue necrosis (i.e., severe necrotizing enterocolitis). This must be addressed by correcting the underlying cause of acidosis and by giving sodium bicarbonate. Fluids lost through nasogastric suctioning or drainage must be replaced at regular intervals by normal saline with maintenance potassium added; if losses are from the small intestine, it has been recommended that a small amount of bicarbonate be also added. Where large fluid losses occur from aspiration, calculation of the electrolyte content of these fluids may help plan replacement (Table 13.3). 87,88
Critical Care Flight Nurses' role within secondary aeromedical services and the inter-hospital transfer of patients with acute spinal cord impairment
Published in Contemporary Nurse, 2023
Heather McCurdy
Respiratory failure and hypoxia are conditions to which patients with SCI are particularly susceptible and that will be exacerbated by transport in the aeromedical environment. Pre-flight assessment of Mr X revealed that he was tachypneic, had increased work of breathing, a paradoxical pattern of breathing in the chest and abdomen and was receiving supplemental oxygen via High Flow Nasal Prongs (HFNP) at 50% Fraction of Inspired Oxygen (FiO2). Arterial blood gas showed an uncompensated respiratory acidosis. Patients with CSI at or above C5, are prone to respiratory failure due to denervation of the phrenic nerve resulting in paralysis or weakness of the diaphragm, intercostal and abdominal muscles (Wang et al., 2021; Life In The Fast Lane (LITFL), 2020). This results in reduced lung and chest wall compliance, hypoventilation and ultimately a mismatch between Ventilation and Perfusion (V/Q) (American College of Surgeons, 2018; Bersten et al., 2019). To optimise patients for transport and to prevent exacerbation of hypoxia and clinical deterioration at altitude, CCFN must have a sound understanding of hypoxia, hypoxemia and how decreased barometric pressure at altitude affects the diffusion of oxygen.
Severe bark scorpion envenomation in adults*
Published in Clinical Toxicology, 2018
Ayrn D. O’Connor, Angela Padilla-Jones, Anne-Michelle Ruha
A 65-year-old woman with history of chronic daily ethanol use presented after a witnessed scorpion envenomation to the left knee. She developed paresthesias preventing ambulation, opsoclonus, myoclonic jerks and hypertensive crisis (BP 209/107 mmHg). Lorazepam and fentanyl were utilized to control signs of envenomation. Additional findings on admission included hyponatremia (Na+ nadir 123; ref 135–145 mmol/L) and hypokalemia (K+ nadir 3.0; ref 3.5–5.2 mmol/L), which were likely unrelated to envenomation. Blood pressure control necessitated use of hydralazine and clonidine. Mild respiratory acidosis developed approximately 5 h after arrival. The patient developed significant encephalopathy, mild respiratory distress with hypoxia which required transfer to the ICU and treatment with supplemental oxygen, albuterol and ipratropium. Although titration of lorazepam and fentanyl likely contributed to respiratory distress, the etiology of the patient’s encephalopathy was considered multifactorial (iatrogenic sedation, ethanol withdrawal, hyponatremia, hypertensive encephalopathy were all cited as possible contributing factors) and not ascribed to the envenomation. Rhabdomyolysis (peak CK 1409; ref 32–235 IU/L) also occurred. The patient was discharged home following a length of stay of 60 h.
Approach to the patient presenting with metabolic acidosis
Published in Acta Clinica Belgica, 2019
Jill Vanmassenhove, Norbert Lameire
Acidosis can be either metabolic (primary change is in the plasma bicarbonate), respiratory (primary change is in the pCO2) or both. In primary acute metabolic acidosis, in the absence of associated ventilatory problems, one expects a fall in arterial pCO2 of 1 mmHg from 40 for every mmol/l fall in pHCO3− from 25. If the arterial pCO2 is much higher than expected, a coexistent ventilation type of respiratory acidosis is present. In contrast, if the arterial pCO2 is much lower than expected, concomitant respiratory alkalosis is also present. We refer to the paper by Adrogue et al for a more in-depth study of the expected responses to primary acid base disorders [11]. For correct interpretation of the lab data, the clinical picture must always be integrated. For example, the finding of acidemia, a high arterial pCO2 and an elevated pHCO3- does not indicate that chronic respiratory acidosis is present in absence of a clinical chronic pulmonary condition. The more likely diagnosis is metabolic alkalosis with an acute respiratory acidosis.
Related Knowledge Centers
- Acidosis
- Bicarbonate
- Carbon Dioxide
- Ph
- Renal Compensation
- Hypoventilation
- Hypercapnia
- Pulmonary Alveolus
- Pco2
- Control of Ventilation